1. Nematoda VMP 920 Infection & Immunity II Veterinary Parasitology

2. Haemonchus contortus Barber-pole worm (Haemonchosis) Morphology Dimorphic Male (bursate) & Female Nematodes

3. Life Cycle Life cycle image

4. Life Cycle Direct Life Cycle (Goats & Sheep - abomasum) Transmission -- ingestion of infective larvae (L3) (deadly dew-drop) From eggs in feces to infective L3 takes 4-6 days on pasture Pasture-borne parasite 3 week prepatency But peracute dz in young hosts in less than 1 week

5. Life Cycle Arrested (hypobiotic) larvae in host Survive harsh seasons Periparturient rise “targets” very young animals Premunition Inhibits development of arrested larvae May result in Post-treatment DZ

6. Pathology Hemorrhagic anemia Hypoproteinemia Severe pallor (anemia) Facial edema “Bottle-jaw”

7. Pathology Morbidity & Mortality

8. Pathology @ necropsy Severe pallor (anemia) throughout organs Very thin, non-clotting blood Abundant worms in abomasum

9. Pathology – Peracute DZ “extremely large number of immature worms” FWEC = 0 epg to very low epg (eggs per gram of feces) young goats, lambs exsanguinated before worms mature. Severe hemorrhagic gastritis. May remove 1/5 of circulating erythrocyte volume per day. Sudden death from acute blood loss.

10. Pathology – Acute DZ 1,000 to 10,000 worms FWEC = As high as 100,000 epg Young susceptible animals become heavily infected. Anemia develops rapidly. Expansion of the erythropoietic response. Generalized anemia and hypoproteinemia. May remove 1/10 of circulating erythrocyte volume per day.

11. Pathology – Chronic DZ 100 to 1,000 worms FWEC = <2,000 epg Older animals 100% morbidity but low mortality Morbidity depends on animal’s erythropoietic capacity, iron and nutritional metabolic reserves. Anemia & Hypoproteinemia may or may not be severe.

12. Clinical Signs & Diagnosis Signs of anemia, tarry feces, pale mucus membranes, bottle-jaw, (not diarrhea) McMasters = Fecal Worm Egg Count (FWEC) At what FWEC would you treat? Resistance/Efficacy check with McMasters. FAMACHA = “Grade” of pale mucous membranes

13. Clinical Signs & Diagnosis SHEEP or GOAT

14. Clinical Signs & Diagnosis Normal feces

15. Clinical Signs & Diagnosis McMasters Quantitation Fecal Worm Egg Count (FWEC) Strongyle-type eggs

16. Clinical Signs & Diagnosis FAMACHA is an acronym derived from the name of the creator of this system, Dr. Faffa Malan; CHA stands for chart. FAMACHA For Grading pallor of mucous membranes

17. Treatment Fenbendazole, Pyrantel, Ivermectin, etc. Dewormer Resistance a major problem Spring treatment of pregnant females to target periparturient rise.

18. Control Pasture “Sanitation” (impractical) Regular scheduled Deworming [Ex. Deworm monthly] (may result in resistance) Pasture rotation (requires 2-6 month rest => much land needed) Co-species grazing Test (McMasters) & Treat (selective deworming) FAMACHA, Test & Treat (selective deworming) – provides refugia => inhibit large population of resistant worms. - slows development of resistant worm population

19. Control: McMasters McMasters Quantitation Strongyle-type eggs Use for making selective deworming decisions deter resistance & promote refugia Use to identify hosts that shed a lot of worm eggs Use to determine dewormer efficacy

20. Control: FAMACHA Use for tactical deworming Use for making selective deworming decisions deter resistance & promote refugia

21. Control Refugia image

22. Challenges to Control Infective Larvae on Pasture Hypobiotic Larvae in Host Worm resistance to Dewormers Prevent “contamination” of pasture & host through selective strategic deworming.

23. Important Points Direct Life Cycle – Pasture-borne parasite (L3) (deadly-dewdrop)  Sanitation by deworming strategy. Special life cycle concerns: Prepatent period, Hypobiotic larvae  “overwinter”, Peripartureint rise  targets neonates. Blood-feeding worms  Pathology (Peracute, Acute, Chronic)  anemia. Clinical Signs. Diagnostics: Response to treatment, McMasters & FWEC, FAMACHA Control: Advantages & disadvantages of each control strategy. Control: Understand concept of refugia to inhibit resistant populations

24. Equine Small Strongyles over 40 species Dimorphic Male (bursate) & Female Nematodes

25. Life Cycle Life cycle image

26. Life Cycle Direct Life Cycle (Horse – large intestine) Transmission -- ingestion of infective larvae (L3) (deadly dew-drop) From eggs in feces to infective L3 takes 4-6 days on pasture Pasture-borne parasite 2.5 to 3 months prepatency

27. Life Cycle Arrested (hypobiotic) larvae in host Premunition inhibits development “prepatency” of arrested larvae - as few as 18 days post-reactivation Post-treatment DZ Periparturient rise “targets” very young animals

28. Pathology Mainly caused by emerging larvae. Acute -- severe enteritis & diarrhea, hypoalbuminemia Post-treatment -- severe enteritis, colitis & diarrhea, hypoalbuminemia Chronic -- granulomatous colitis

29. ACUTE

33. Pathology Severe Colitis

34. Clinical Signs & Diagnosis Persistent diarrhea, edema, poor body condition, COLIC McMasters = Fecal Worm Egg Count (FWEC) At what FWEC would you treat? Will only show adult burden, not DZ causing emerging larvae. Resistance check with McMasters.

35. Clinical Signs Signs of colic Diarrhea

36. Diagnosis McMasters Quantitation Fecal Worm Egg Count (FWEC) Strongyle-type eggs (maybe negative in acute pathology)

37. Treatment Fenbendazole, Pyrantel, Ivermectin, etc. Dewormer Resistance a major problem

38. Control Pasture “Sanitation” (removal of feces) Regular scheduled Deworming [Ex. Deworm every 2 months] (may result in resistance) Pasture rotation (requires months of rest => much land needed) Co-species grazing Test (McMasters) & Treat – provide refugia => inhibit large population of resistant worms. - slows development of resistant worm population

40. Challenges to Control Infective Larvae on Pasture Hypobiotic Larvae in Host Worm resistance to Dewormers Prevent “contamination” of pasture & host through selective strategic deworming.

41. Important Points Direct Life Cycle – Pasture-borne parasite (L3) (deadly-dewdrop)  Sanitation by deworming strategy. Special life cycle concerns: Prepatent period  adult worms & Arrested larvae, Hypobiotic larvae  “overwinter”, Peripartureint rise  target young, Premunition + Arrested larvae  Post- treatment DZ Emerging larvae  Pathology (Acute, Post-treatment, Chronic), Clinical Signs – COLIC, Enteritis Diagnostics: McMasters & FWEC, Control: Advantages & disadvantages of each control strategy. Control: Understand concept of refugia to inhibit resistant populations